White lesions (2)

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White lesions (2)

  1. 1. WHITELESIONS Prepared by: Dr. Rea Corpuz
  2. 2. White Lesions lesions of the oral mucosa, which are white results from a  thickened layer of keratin  epithelial hyperplasia  intracellular epithelial edema  reduced vascularity of subjacent connective
  3. 3. White Lesions white or yellow lesions may also be due to fibrous exudate covering an:  ulcer  submucosal deposit  surface debris  fungal colonies
  4. 4. White Lesions (1) Leukoedema (2) Leukoplakia (3) Lichen Planus (4) Candidiasis (5) White Sponge Nevus (6) Nicotine Stomatitis
  5. 5. White Lesions (7) Geographic Tongue (8) Hairy Tongue (9) Dental Lamina Cyst (10) Fordyce’s Disease (11) Perleche
  6. 6. (1) Leukoedema generalized opacification of buccal mucosa that is regarded as a variation of normal can be identified in majority of population
  7. 7. (1) Leukoedema Etiology & Pathogenesis  to date, cause has not been established  smoking  chewing tobacco none  alcoholo ingestion are  bacterial infection proven  salivary condition cause  electrochemical interactions have been implicated
  8. 8. (1) Leukoedema Clinical Features  usual discovered as incidental finding  asymptomatic  symmetrically distributed in buccal mucosa
  9. 9. (1) Leukoedema Clinical Features  appear as gray-white, diffuse, filmy or milky surface  more exaggerated cases, whitish cast with surface textural changes • wrinkling • or corrugations
  10. 10. (1) Leukoedema Clinical Features  with stretching of buccal mucosa, opaque changes dissipate  more apparent in non-whites, especially African-American
  11. 11. (1) Leukoedema Treatment  NO treatment is necessary  since there is no malignant potential  if there is any doubt about diagnosis, a biopsy can be performed
  12. 12. (2) Leukoplakia also known as Leukokeratosis; Erythroplakia Leuko= white Plakia = patch defined by World Health Organization (WHO) as a white patch or plaque that cannot be characterized clinically or pathologically as any other disease
  13. 13. (2) LeukoplakiaLeukoplakia clinical term indicating a white patch or plaque of oral mucosa cannot be rubbed off cannot be characterized clinically as any other disease biopsy is mandatory to establish a definitive diagnosis
  14. 14. (2) Leukoplakia Mild or Thin Leukoplakia Homogenous or Thick Leukoplakia Granular or Nodular Leukoplakia Verrucous or Verruciform Leukoplakia
  15. 15. (2) Leukoplakia Proliferative Verrucous Leukoplakia (PVL) Erythroleukoplakia or Speckled Leukoplakia
  16. 16. (2) Leukoplakia
  17. 17. (2) Leukoplakia Mild or Thin Leukoplakia  seldom shows dysplasia on biopsy  may disappear or continue unchanged
  18. 18. (2) Leukoplakia Homogenous or Thick Leukoplakia  for tobacco smokers who do not reduce their habit  2/3 of such lesions slowly extend laterally, become thicker + acquire distinctly white appearance
  19. 19. (2) Leukoplakia Homogenous or Thick Leukoplakia  affected mucosa may become leathery to palpation  fissures may deepen  become more numerous  most thick, smooth lesions remain indefinitely at this stage
  20. 20. (2) Leukoplakia Homogenous or Thick Leukoplakia  some, perhaps as many as 1/3, regress or disappear
  21. 21. (2) Leukoplakia Granular or Nodular Leukoplakia  few become even more severe  develop increased surface irregularities
  22. 22. (2) Leukoplakia Verrucous or Verruciform Leukoplakia  lesions that demonstrate sharp or blunt projections
  23. 23. (2) Leukoplakia Proliferative Verrucous Leukoplakia (PVL)  high risk form of leukoplakia  development of multiple keratotic plaques  with roughened surface projections
  24. 24. (2) Leukoplakia Proliferative Verrucous Leukoplakia (PVL)  tend to slowly spread  involve additional oral mucosal sites  gingiva is frequently involved  although other sites may be affected as well
  25. 25. (2) Leukoplakia Proliferative Verrucous Leukoplakia (PVL)  as lesions progress, there may go through a stage indistinguishable  transform into full-fledged squamous cell carcinoma (usually within 8 years of initial PVL diagnosis)
  26. 26. (2) Leukoplakia Proliferative Verrucous Leukoplakia (PVL)  lesions rarely regress despite therapy  strong female predilection  minimal association with tobacco use
  27. 27. (2) Leukoplakia Erythroplakia  leukoplakia may become dysplastic  even invasive, with no change in its clinical appearance  however, some lesions eventually demonstrate scattered patches of redness called erythroplakia
  28. 28. (2) Leukoplakia Erythroleukoplakia or Speckled Leukoplakia  such areas usually represent sites in which epithelial cells are so immature or atrophic that they can no longer produce keratin
  29. 29. (2) Leukoplakia Erythroleukoplakia or Speckled Leukoplakia  intermixed red-and-white lesion  pattern of leukoplakia that frequently reveals advanced dysplasia on biopsy
  30. 30. (2) Leukoplakia Etiology & Prognosis  many cases are etiologically related to use of tobacco in smoked or smokeless forms and may regress after discontinuation of tobacco use
  31. 31. (2) Leukoplakia Etiology & Prognosis  other factors, such as • alcohol abuse may have • trauma a role in • C. albicans infection etiology
  32. 32. (2) Leukoplakia Etiology & Prognosis  nutritional factors have been cited as important, especially iron deficiency anemia
  33. 33. (2) Leukoplakia Clinical Features  associated with middle-aged + older population  vast majority of cases occur after age of 40 years
  34. 34. (2) Leukoplakia Site of Occurence  Vestibule  Buccal  Palate  Alveolar Ridge  Lip  Tongue  Floor
  35. 35. (2) Leukoplakia leukoplakia of lips + tongue also exhibits relative high percentage of dysplastic or neoplastic change
  36. 36. (2) Leukoplakia Treatment & Prognosis  absence of dysplastic or atypical epithelial changes • periodic examinations + rebiopsy of new suspicious areas are recommended
  37. 37. (2) Leukoplakia Treatment & Prognosis  if diagnosis as moderate to severe dysplasia • excision is obligatory  for large lesions, grafting procedures may be necessary after surgery  may recur after complete removal
  38. 38. (3) Lichen Planus chronic mucocutaneous disease of unknown cause relatively common typically presents as bilateral white lesions occasionally with associated ulcers
  39. 39. (3) Lichen Planus Pathogenesis  although cause is unknown  generally considered to be a immunologically mediated process  resembles hypersensitivity reaction
  40. 40. (3) Lichen Planus Clinical Features  disease of middle age  affects men + women in nearly equal numbers  children rarely affected
  41. 41. (3) Lichen Planus Clinical Features  Types: • Reticular • Erosive (ulcerative) • Plaque • Papular • Erythematous (atrophic)
  42. 42. (3) Lichen Planus Clinical Features  Reticular Form • most common type • numerous interlacing white keratotic lines or striae (Wickham’s striae)  produces anular or lacy pattern
  43. 43. (3) Lichen Planus Clinical Features  Reticular Form • buccal mucosa is the site most commonly involved • may also be noted on:  tongue  gingiva – less common  lips
  44. 44. (3) Lichen Planus Clinical Features  Plaque Form • resembles leukoplakia • but has multifocal distribution • range from slightly elevated to smooth and flat
  45. 45. (3) Lichen Planus Clinical Features  Plaque Form • primary sites are  dorsum of tongue  buccal mucosa
  46. 46. (3) Lichen Planus Clinical Features  Erythematous Form • red patches • with very fine white striae • attached gingiva commonly involved
  47. 47. (3) Lichen Planus Clinical Features  Erythematous Form • patchy distribution often in four quadrants • patient may complain of  burning  sensitivity  generalized discomfort
  48. 48. (3) Lichen Planus Clinical Features  Erosive Form • central area of lesion is ulcerated • fibrinous plaque or pseudomembrane covers ulcer • changing patterns of involvement from week to week
  49. 49. (3) Lichen Planus Treatment  although it cannot be generally cured  some drugs can provide satisfactory control  corticosteroids are the single most useful group of drugs in the management of lichen planus
  50. 50. (3) Lichen Planus Treatment  corticosteroid • ability to modulate inflammation + immune response
  51. 51. (3) Lichen Planus Treatment  topical application + local injection of steroids have been used successfully in controlling but not curing this disease
  52. 52. (4) Candidiasis common oppurtunistic oral mycotic infection develops in the presence of one of several predisposing factors • immunodeficiency • endocrine disturbances • hypoparathyroidism • diabetes mellitus • poor oral hygiene • xerostomia
  53. 53. (4) Candidiasis caused by Candida albicans infection with this organism is usually superficial, affecting the outer aspects of involved oral mucosa or skin
  54. 54. (4) Candidiasis in severely debilitated + immunocompromised patients such as patients with AIDS  infection may extend into alimentary tract (candidal esophagitis  bronchopulmonary tract  and other organ system
  55. 55. (4) Candidiasis Clinical Features  most common form is acute pseudomembranous also known, as thrush • young infants + elderly are commonly affected
  56. 56. (4) Candidiasis Clinical Features  oral lesion of acute candidiasis (thrush) • white • soft plaques that sometime grow centrifugally + merge • wiping plaques with gauze sponge leaves a painful, eroded, eryhtematous or ulcerated surface
  57. 57. (4) Candidiasis Clinical Features  Chronic Erythematous Candidiasis • commonly seen on geriatric individuals • who wear complete maxillary denture
  58. 58. (4) Candidiasis Clinical Features  Chronic Erythematous Candidiasis • distinct predilection for palatal mucosa as compared with mandibular alveolar arch
  59. 59. (4) Candidiasis Clinical Features  Chronic Erythematous Candidiasis • chronic low-grade resulting from poor prosthesis fit • failure to remove appliance at night
  60. 60. (4) Candidiasis Clinical Features  Chronic Erythematous Candidiasis • bright red • relative little keratinization
  61. 61. (4) Candidiasis Clinical Features  Hyperplastic Candidiasis • may involve dorsum of tongue • pattern referred to as median rhomboid glossitis
  62. 62. (4) Candidiasis Clinical Features  Hyperplastic Candidiasis • usually asymptomatic • usually discovered on routine oral examination
  63. 63. (4) Candidiasis Clinical Features  Hyperplastic Candidiasis • found anterior to circumvallate papillae • oval or rhomboid outline
  64. 64. (4) Candidiasis Clinical Features  Hyperplastic Candidiasis • may have smooth, nodular or fissured surface • range in color from white to more red
  65. 65. (4) Candidiasis Clinical Features  Mucocutaneous Candidiasis • long standing • persistent candidiasis of  oral mucosa  skin  vaginal mucosa
  66. 66. (4) Candidiasis Clinical Features  Mucocutaneous Candidiasis • often resistant to treatment • begins as a pseudomembranous type of candidiasis • soon followed by nail + cutaneous involvement
  67. 67. (4) Candidiasis Treatment  majority of infections may be simply treated with topical applications of nystatin suspension • nystatin cream or ointment often effective when applied directly to denture-bearing surface itself
  68. 68. (4) Candidiasis Treatment  topical applications of either nystatin or clotrimazole should be continued for at least 1 week beyond disappearance of clinical manifestations of disease
  69. 69. (4) Candidiasis Treatment  Hyperplastic Candidiasis • topical + systemic antifungal agents may not be effective at completely removing lesions  surgical management may be necessary
  70. 70. (4) Candidiasis Treatment  Chronic Mucocutaneous Candidiasis associated with immunosuppression • topical agents may not be effective
  71. 71. (4) Candidiasis Treatment  Chronic Mucocutaneous Candidiasis associated with immunosuppression • systemic administration of medications:  Ketoconazole  Fluconazole  Itraconazole
  72. 72. (5) White Sponge Nevus autosomal-dominant condition due to point mutations for genes coding for keratin 4 and/or 13. affects oral mucosa bilaterally NO treatment is required
  73. 73. (5) White Sponge Nevus Clinical Features • asymptomatic • folded white lesions • may affect several mucosal sites • lesions tend to be thickened + spongy consitency
  74. 74. (5) White Sponge Nevus Clinical Features • presentation intraorally is almost always bilateral + symmetric • usually appears early in life, typically before puberty
  75. 75. (5) White Sponge Nevus Clinical Features • usually observed in buccal mucosa • tongue + vestibular mucosa may be involved
  76. 76. (5) White Sponge Nevus Treatment • NO treatment necessary since it is asymptomatic + benign
  77. 77. (6) Nicotine Stomatitis common tobacco-related form of keratosis typically associated with pipe + cigar smoking with positive correlation between intensity of smoking + severity of condition
  78. 78. (6) Nicotine Stomatitis combination of tobacco carcinogens + heat is markedly intensified in reverse smoking (lit end positioned inside the mouth) adding a significant risk for malignant conversion
  79. 79. (6) Nicotine Stomatitis Clinical Features  palatal mucosa initially responds with an erythematous change follwed by keratinization
  80. 80. (6) Nicotine Stomatitis Clinical Features  subsequent to opacification or keratinization of palate • red dots surrounded by white keratotic rings appear  dot represent inflammation of salivary gland excretory duct
  81. 81. (6) Nicotine Stomatitis Treatment  condition rarely evolves into malignancy  except in individuals who reverse smoke  discontinuation of tobacco habit
  82. 82. (7) Geographic Tongue also known as erythema migrans, benign migratory glossitis prevalent among whites + blacks strongly associated with fissure tongue inversely associated with cigarette smoking
  83. 83. (7) Geographic Tongue emotional stress may enhance the process
  84. 84. (7) Geographic Tongue Clinical Features  affects women slightly more than men  children occasionally may be affected  characterized initially by presence of atrophic patches surrounded by elevated keratotic margins
  85. 85. (7) Geographic Tongue Clinical Features  desquamated areas appear red + may be slightly tender  followed over a period of days or weeks, pattern changes  appearing to move across dorsum of tongue
  86. 86. (7) Geographic Tongue Clinical Features  most patients are asymptomatic  occasionally patients complain of irritation or tenderness  especially in relation to consumption of spicy foods + alcoholic beverages
  87. 87. (7) Geographic Tongue Clinical Features  lesions periodically disappear  recur for no apparent reason
  88. 88. (7) Geographic Tongue Treatment  NO treatment is required because of self-limiting + usually asymptomatic nature of this condition
  89. 89. (7) Geographic Tongue Treatment  when symptoms occur, • topical steroids especially ones containing antifungal agent  helpful in reducing symptoms
  90. 90. (7) Geographic Tongue Treatment  mouth clean using mouthrinse composed of sodium bicarbonate in water  reassure patients that condition is totally benign
  91. 91. (8) Hairy Tongue clinical term referring to a condition of filiform papillae overgrowth on dorsal surface of tongue there are numerous initiating or predisposing factors for hairy tongue
  92. 92. (8) Hairy Tongue broad spectrum antibiotics such as penicillin + systemic cortiocosteroids are often identified in clinical history of patients with this condition
  93. 93. (8) Hairy Tongue oxygenating mouthrinses containing:  hydrogen peroxide  sodium perborate  carbamide peroxide  have been cited as possible etiologic agents
  94. 94. (8) Hairy Tongue Clinical Features  clinical alteration translates to hyperplasia of filiform papillae; result is • thick serves to trap • matted surface bacteria, fungi, foreign materials
  95. 95. (8) Hairy Tongue Clinical Features  extensive elongation of papillae occurs, • gagging may be • tickiling sensation felt
  96. 96. (8) Hairy Tongue Clinical Features  color may range from white to tan to deep brown depending on: • diet • oral hygiene • composition of bacteria inhabiting papillary surface
  97. 97. (8) Hairy Tongue Treatment  brush/scrape tongue with baking soda  maintain good oral hygiene  emphasize to patients that this process is entirely benign
  98. 98. (8) Hairy Tongue Treatment  self-limiting  tongue should return to normal after institution of physical debridement + proper oral hygiene
  99. 99. (9) Dental Lamina Cyst also known as Gingival Cyst of New Born or Bohn’s nodules appear as multiple nodules along alveolar ridge in neonates
  100. 100. (9) Dental Lamina Cyst similar epithelial inclusion cysts may occur along midline of palate (palatine cyst of new born or Epstein’s pearls)  developmental origin  derived from epithelium  included in fusion line between palatal shelves + nasal processes  no treatment; resolve spontaneously
  101. 101. (9) Dental Lamina Cyst Treatment  not necessary because nearly all spontaneously rupture before patient is 3 months of age
  102. 102. (10) Fordyce’s Granules represents ectopic sebaceous glands or sebaceous choristomas  normal tissue in abnormal location regarded as developmental considered a variation of normal
  103. 103. (10) Fordyce’s Granules multiple often seen in aggregates sites of predilection include • buccal mucosa • vermillion of upper lip
  104. 104. (10) Fordyce’s Granules lesions generally are symmetrical distributed tend to become obvious after puberty maximal expression occurring between 20-30 years of age
  105. 105. (10) Fordyce’s Granules lesions are asymptomatic discovered during routine oral examination
  106. 106. (10) Fordyce’s Granules Treatment  No treatment is indicated • glands are normal in character • do not cause any untoward effects
  107. 107. (11) Perleche also known as Angular Cheilitis inflammation + atrophy of skin of folds at angles of mouth
  108. 108. (11) Perleche may be due to:  excessive lip licking  thumb sucking  sagging of facial skin in edentulous or elderly persons
  109. 109. (11) Perleche may be due to:  prolonged contact with saliva results in maceration  with possible secondary infection by Candida or staphylococci
  110. 110. (11) Perleche Clinical Features  skin at angles of mouth has erythematous fissures  often with exudate + crust  further licking to moisten inflamed area exacerbates the problem
  111. 111. (11) Perleche Treatment  applying antimicrobial creams  followed by low-potency steroid creams until symptoms resolve  protective lip balm may help prevent recurrence
  112. 112. References: Books  Cawson, R.A: Cawson’s Essentials of Oral Oral Pathology and Oral Medicine, 8th Edition • (page 165-167 )  Neville, et. al: Oral and Maxillofacial Pathology 3rd Edition • (pages 388- 397; 590-592; 819-820) Regezi, et. al: Oral Pathology: Clinical Pathologic Correlations, 5th Edition • (pages 73-105; 241-242; 296-299; 394)

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